Table 1.

Genetically-engineered mice models with altered TJ protein expression.

Animal	Gene alteration	GI phenotypes	Other phenotypes	References
Occludin−/−	Global occludin deletion	Chronic gastric inflammation, no significant anomaly in intestinal epithelium	Growth retardation, brain calcification, testicular atrophy, salivary gland dysfunction, and compact bone weakening	[15, 16]
JAM-1−/−	Global JAM-1 deletion	Normal epithelial architecture but increased leukocyte infiltration, increased mucosal permeability		[28]
Tie-2-Cre-JAM-1−/−	Endothelial/haematopoietic -specific JAM deletion	Similar phenotypes as JAM-1−/−		[29]
Cldn1−/−	Global claudin-1 deletion		Dehydration, die on postnatal d 1	[33]
Cl−1Tg	Villin-claudin-1 transgenic mice (Intestinal claudin-1 overexpression)	Increased intestinal epithelial proliferation, inhibited goblet cell differentiation		[9]
APC-Cldn1	APCmin mice crossed with Villin-claudin-1 transgenic mice	Enlarged colon tumor size, reduced mucosal defense related genes	Decreased mouse survival rate	[34]
Cldn2−/−	Global claudin-2 deletion	Reduced intestinal permeability for Na+ and K+, enhanced experimental colorectal inflammation		[10, 44]
Cl−2TG	Villin-claudin-2 transgenic mice (Intestinal claudin-2 overexpression)	Protected against experimental colitis, increased colonocyte proliferation		[46]
Cldn7−/−	Global claudin-7 deletion	Intestinal inflammation, mucosal ulcerations	Salt wasting, dehydration, and growth retardation, die within 12 d	[11]
cCldn7−/−	Intestinal claudin-7 deletion	Colon inflammation	die within 28 d	[48]
Cldn15−/−	Global claudin-15 deletion	Mega-intestine, reduced intestinal permeability for Na+ and K+		[12, 44]
EpCAM−/−	Global EpCAM deletion (LoxP sites are inserted into exon 2 and 3)	Intestinal hemorrhage, obstruction and perforation. Down-regulation of claudins 2, 3, 7, and 15 and impaired TJ barrier function	Most die within 10 d	[13]
EpCAMβgeo/βgeo	Global EpCAM deletion (LoxP sites are inserted into intron 1 and 3)	Same as EpCAM−/−	Same as EpCAM−/−	[13]
EpCAMΔ4/Δ4	Universal EpCAM exon 4 deletion (LoxP site at exon 4)	Congenital tufting enteropathy, blunting of the intestinal villi, intestinal permeability defects	Neonatal lethality and growth retardation. Die within 7 d	[54]
mTrop1/EpCAM	Global mTrop1/EpCAM deletion (Gene-trapping method)	Intestinal tufts, villous atrophy, colon crypt hyperplasia	Neonatal lethality and growth retardation, die within 4 d	[55]